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. Author manuscript; available in PMC: 2018 Jun 22.
Published in final edited form as: Oncogene. 2017 Dec 22;37(10):1279–1292. doi: 10.1038/s41388-017-0032-z

Figure 4. FOXO3a, a downstream target of AMPK, inhibits GOF mutant p53-mediated FOXM1 expression in HNSCC cells.

Figure 4

(A) Ingenuity Pathway Analysis of possible upstream transcription factors regulating FOXM1 expression. (B) Western blot analysis of CRISPR-Cas9/FOXO3a KO UM-SCC-1 cell lines in the presence or absence of metabolic stress under the confluent high-density culture condition. (C) Western blot analysis of isogenic UM-SCC-1 stable cell lines in the presence or absence of metabolic stress under the confluent high-density culture condition. pBMN-EV, empty vector. (D) Real-time RT-qPCR analysis of mRNA transcripts of FOXM1b and -1c from UM-SCC-1 stable cells under the confluent high-density culture condition. *, <0.05; **, p<0.01. pLVX-EV, empty vector. (E) Western blot analysis of Detroit 562 stable cell lines in the presence or absence of metabolic stress under the confluent high-density culture condition. (F) Real-time RT-qPCR analysis of FOXM1b mRNA transcripts from Detroit 562 stable cells in the presence or absence of metabolic stress under the confluent high-density culture condition. *, <0.05; **, p<0.01.